scholarly journals CHEMICAL TRANSMISSION AND ADAPTATION

1957 ◽  
Vol 40 (4) ◽  
pp. 533-545 ◽  
Author(s):  
Ernst Florey
Keyword(s):  
Sensory Neurons ◽  
Time Course ◽  
Silent Period ◽  
Nerve Fibers ◽  
Sudden Increase ◽  
Impulse Frequency ◽  
Factor I ◽  
Central Neurons ◽  
Frequency Level ◽  
Sudden Decrease

Acetylcholine and factor I appear to be transmitter substances of excitatory and inhibitory regulatory nerve fibers supplying the sensory neurons of stretch receptor organs of the crayfish. Sudden application of a low concentration of acetylcholine causes the impulse frequency to jump to a peak value. But immediately the frequency falls again and gradually reaches a steady state which is not far above the previous frequency level. If the acetylcholine is now withdrawn there follows a silent period after which the frequency returns to its original level. The time course of these events is identical with that of adaptations to sudden increase or decrease of stretch. Factor I in sufficiently low concentrations causes an immediate fall in impulse frequency (silent period) which is followed by a return to a value near the previous frequency level. Withdrawal of factor I is followed by excitation and again return of the frequency to the rate measured before the application of factor I. The time course of these phenomena is identical with that of adaptations to sudden decrease and increase of stretch. It is suggested that adaptation may be a property not only of sensory neurons but of neurons in general and that even central neurons may be considered as receptor neurons inasmuch as they respond to chemically transmitted excitatory and inhibitory stimuli.

Neural mechanisms in vibrotactile adaptation

1988 ◽  
Vol 59 (2) ◽  
pp. 607-622 ◽  
Author(s):  
S. O'Mara ◽  
M. J. Rowe ◽  
R. P. Tarvin
Keyword(s):  
Time Course ◽  
Sensory Nerve ◽  
Dorsal Column ◽  
Nerve Fibers ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Central Neuron ◽  
Similar Time ◽  
Central Neurons

1. Peripheral and central neural contributions to vibrotactile adaptation were investigated in decerebrate or anesthetized cats by recording from sensory nerve fibers associated with Pacinian corpuscle (PC) receptors and from central neurons of the dorsal column nuclei that receive their input from vibration-sensitive receptors of the forelimb footpads. Responsiveness of units was assessed using 1-s duration, test vibration stimuli delivered with 1- to 2-mm-diam probes at different times following adapting trains of vibration (usually 300 Hz) that lasted from less than 1 min up to 50 min. 2. Cuneate neuron responsiveness underwent marked depression following prior vibration. The extent of the depression and the time course of recovery in responsiveness were dependent on the intensity and duration of the adapting vibratory stimulus. The recovery time course (often several minutes) was approximately exponential and resembled the reported time course of subjective vibrotactile adaptation obtained in psychophysical experiments. 3. Response depression in PC fibers was only seen at low amplitudes of the test vibration and displayed a brief time course of recovery in comparison with that seen in cuneate neurons. It is therefore unlikely to account for the adaptation time course either in cuneate neurons or at a subjective level. Furthermore, as the adaptation seen in PC fiber responses had a similar time course in both cutaneous and mesenteric PC fibers it is unlikely that mechanical changes in the skin contribute significantly to the adaptation in PC fiber responses to vibration. 4. The time course of afferent-induced inhibition following long periods of prior vibration was too brief to account for the response adaptation in cuneate neurons. 5. As the long-term response depression in cuneate neurons following their prior activation was seen for inputs from unconditioned sites within the neuron's excitatory receptive field, as well as from the conditioned site, it appears that the response adaptation is attributable to changes in the central neuron or in synaptic processes associated with the central neuron. It is proposed that this adaptation may be due to an increase in extracellular potassium ion concentration that alters the responsiveness of the central neurons.

Is cyclic guanosine monophosphate the internal 'second messenger' for cholinergic actions on central neurons?

1976 ◽  
Vol 54 (2) ◽  
pp. 172-176 ◽  
Author(s):  
K. Krnjević ◽  
E. Puil ◽  
R. Werman
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Resting Potential ◽  
Electrical Excitability ◽  
Spinal Motoneurons ◽  
Central Neurons ◽  
Intracellular Cgmp ◽  
Post Synaptic Potential

The most consistent effects produced by intracellular injections of guanosine 3′,5′-cyclic monophosphate (cGMP) (but not 5′-guanosine 5′-monophosphate in spinal motoneurons of cats are a rise in membrane conductance, acceleration in time course of spike potentials, and accentuation of the post-spike hyperpolarization. Associated changes in resting potential are smaller, less constant, and more often in the depolarizing than hyperpolarizing direction. cGMP tends to increase electrical excitability but reduces excitatory post-synaptic potential amplitudes. Most of the effects of intracellular cGMP are quite different from, or indeed opposite to, those of either extra- or intracellular applications of acetylcholine and therefore not consistent with the proposal that cGMP is the internal mediator of muscarinic actions.

Time course of exchanges between red cells and extracellular fluid during CO2 uptake

1975 ◽  
Vol 38 (4) ◽  
pp. 710-718 ◽  
Author(s):  
R. E. Forster ◽  
E. D. Crandall
Keyword(s):  
Carbonic Anhydrase ◽  
Time Course ◽  
Extracellular Fluid ◽  
Extracellular Ph ◽  
Co2 Uptake ◽  
Sudden Increase ◽  
Red Cell ◽  
Ph Change ◽  
Red Cell Membrane

A stopped-flow rapid-reaction apparatus was used to follow the time course of extracellular pH in a human red cell suspension following a sudden increase in PCO2. The extracellular pH change was slow (t1/2 similar to 3.5 s) considering the presence of carbonic anhydrase in the cells. When carbonic anhydrase was added to the extracellular fluid, the half-time was reduced to less than 20 ms. The explanation for these phenomena is that the equilibration of H+ across the red cell membrane is rate-limited by the uncatalyzed reaction CO2 plus H2O formed from H2CO3 outside the cells. A theoretical model was developed which successfully reproduced the experimental results. When the model was used to simulate CO2 exchange in vivo, it was determined that blood PCO2 and pH require long times (greater than 50 s) to approach equilibrium between cells and plasma after leaving an exchange capillary. We conclude that cell-plasma equilibrium may never be reached in vivo, and that in vitro measurements of these quantities may not represent their true values at the site of sampling.

Mechanism of secretion of plasma insulin-like growth factor-I into milk of lactating goats

1991 ◽  
Vol 131 (3) ◽  
pp. 459-466 ◽  
Author(s):  
C. G. Prosser ◽  
I. R. Fleet ◽  
A. J. Davis ◽  
R. B. Heap
Keyword(s):  
Growth Factor ◽  
Time Course ◽  
Specific Activity ◽  
Gel Filtration ◽  
Free Form ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Lactating Goats ◽  
Igf I ◽  
Growth Factor I

ABSTRACT 125I-Labelled insulin-like growth factor-I (IGF-I) was infused as the free form directly into the pudic artery supplying one gland of lactating goats (n = 6). The infusion was for 60 min and 0·4±0·09% (s.e.m.) of the infusate was secreted into milk from the infused gland during its first passage through that gland. A large proportion of the 125I-labelled IGF-I escaped into the systematic circulation and was secreted into milk of both glands. A total of 5·2±0·4% of infused radioactivity was recovered in milk from both glands from 0 to 720 min. Radioactivity consisted of trichloroacetic acid (TCA)-precipitable and -soluble counts which were shown by gel filtration to be authentic IGF-I and degraded products of the peptide. The amount and time course of TCA-soluble radioactivity in milk from both glands was similar, suggesting degradation of 125I-labelled IGF-I at extramammary sites. Maximum specific activity for 125I-labelled IGF-I in milk from the infused gland was reached 80–120 min after the start of infusion and was 2·5-fold greater than milk from the non-infused gland. The time course of appearance of 125I-labelled IGF-I in milk suggests that transfer was via the transcellular pathway and this was further supported by comparing the pattern of transfer of [14C]sucrose and [14C]amino acids. When excess unlabelled IGF-I was included in the infusate, specific activity in milk from the infused gland was reduced to that of the non-infused gland, indicating a competitive and saturable mechanism of secretion for 125I-labelled IGF-I. Comparison of uptake and secretion of 125I-labelled IGF-I into milk from the non-infused gland with that of endogenous immunoreactive IGF-I suggests that vectorial transport of IGF-I across the mammary gland may be a significant contributor of IGF-I levels in milk. Journal of Endocrinology (1991) 131, 459–466

Lung inflation: effects on heart rate, respiration, and vagal afferent activity in seals

1981 ◽  
Vol 240 (2) ◽  
pp. H190-H198 ◽  
Author(s):  
J. E. Angell-James ◽  
R. Elsner ◽  
M. De Burgh Daly
Keyword(s):  
Transpulmonary Pressure ◽  
Harbor Seal ◽  
Nerve Fibers ◽  
Cardiac Response ◽  
Impulse Frequency ◽  
Lung Inflation ◽  
Afferent Nerve Fibers ◽  
Close Relationship ◽  
Vagal Afferent ◽  
Carotid Body Chemoreceptors

In the anesthetized harbor seal, Phoca vitulina, the Hering-Breuer inflation reflex was weak and comparable to that in humans. Single inflations of the lungs from a syringe during the expiratory phase of normal breathing caused temporary inhibition of breathing and an immediate tachycardia dependent on the integrity of the cervical vagosympathetic nerves. A similar cardiac response occurred when the lungs were artificially inflated during an experimental dive and under conditions in which apnea and bradycardia were reflexly induced by a combination of stimulation of the carotid body chemoreceptors and of the trigeminal or laryngeal input. Recordings from single vagal afferent nerve fibers innervating presumptive pulmonary stretch receptors showed a close relationship between the increase in impulse frequency and increase in lung volume or transpulmonary pressure. It appears that in diving the decrease in pulmonary stretch receptor activity during apnea, combined with cessation of central inspiratory neuronal drive, is an important integrative mechanism that helps development of the reflex bradycardia of trigeminal, carotid, chemoreceptor, and baroreceptor origin.

Dendritic origin of late events in optical recordings from salamander olfactory bulb

1992 ◽  
Vol 68 (3) ◽  
pp. 786-806 ◽  
Author(s):  
A. R. Cinelli ◽  
B. M. Salzberg
Keyword(s):  
Olfactory Bulb ◽  
Time Course ◽  
Slow Component ◽  
Field Potential ◽  
Olfactory Nerve ◽  
Nerve Fibers ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Direct Stimulation ◽  
Compound Action

1. Optical recordings of membrane-potential changes were used to characterize the origin and properties of the electrical signals from the dendritic level in slices of the salamander olfactory bulb. 2. The optical events were correlated with field-potential waves recorded simultaneously. Both responses exhibited patterns similar to those found in other species. 3. Orthodromic stimulation evoked a compound action potential in the olfactory nerve fibers, followed by two additional principal waves (N1 and N2). These field-potential waves reflected excitatory postsynaptic potentials at the primary mitral/tufted and granule cell dendrites, respectively. 4. Extrinsic optical signals from horizontal slices stained with the pyrazo-oxonal dye RH-155 showed a characteristic sequence of depolarizing and hyperpolarizing events. All of the signals exhibited a wavelength dependence expected for this dye and were abolished in the presence of high K+ in the bath. 5. According to their time courses, depolarizing responses under normal recording conditions were divided into two components, fast and slow. Orthodromic stimuli evoked a fast presynaptic response that represents synchronous compound action potentials from olfactory nerve fibers. At subglomerular levels, additional fast responses could often be recorded at the peri/subglomerular level and in the mitral/tufted somata region. These postsynaptic responses partially coincided with the rising phase of a different depolarizing signal, a slow component characterized by its prolonged time course. 6. With orthodromic stimulation, this slow signal attained its largest amplitude in the zone between the glomeruli and the superficial part of the external plexiform layer (EPL). Antidromic stimuli evoked a signal with some similarities to the one evoked orthodromically, but originating in deeper EPL regions. 7. Slow components were characterized by their Ca dependence. Low Ca2+ medium, or calcium channel blockers, suppressed this optical component, whether evoked orthodromically, antidromically, or by direct stimulation. In addition, Ba2+ (2.5–3.6 mM) in the bath did not abolish these responses, suggesting that they do not reflect a glial depolarization in response to elevated extracellular K+ concentration ([K+]o). 8. Locally applied stimuli next to the glomerular layer elicited these signals in 5–10 microM tetrodotoxin (TTX) or in low extracellular Na+ concentration ([Na+]o) medium, but antidromic or orthodromic stimuli failed to evoke the response under these conditions. The sizes of the responses to local stimuli remained constant, but an increase in their duration was observed in either TTX or low [Na+]o. 9. gamma-Aminobutyric acid (GABA) and baclofen reduced the size of the slow components in a dose-dependent manner.(ABSTRACT TRUNCATED AT 400 WORDS)

Pharmacological and kinetic characterization of two functional classes of serotonergic modulation in Aplysia sensory neurons

1996 ◽  
Vol 75 (2) ◽  
pp. 855-866 ◽  
Author(s):  
L. L. Stark ◽  
A. R. Mercer ◽  
N. J. Emptage ◽  
T. J. Carew
Keyword(s):  
Synaptic Transmission ◽  
Sensory Neurons ◽  
Time Course ◽  
Behavioral Sensitization ◽  
Input Resistance ◽  
Short Term ◽  
Synaptic Facilitation ◽  
Functional Classes ◽  
Kinetics Of ◽  
Serotonergic Modulation

1. Modulation of mechanoafferent sensory neurons (SNs) by the neutrotransmitter serotonin (5HT) plays a significant role in behavioral sensitization of several withdrawal reflexes in Aplysia. The modulatory effects of 5HT on these SNs include increased excitability, increased input resistance, action potential broadening, and increased synaptic transmission. Based on a previously described dissociation of some of these modulatory effects, revealed with the 5HT-receptor antagonist, cyproheptadine, we investigated whether a similar dissociation could be found by systematically varying the concentration of the endogenous agonist, 5HT. 2. We first applied a range of 5HT concentrations to isolated pleural/pedal ganglia (containing tail SNs and tail motor neurons, respectively), and measured the magnitude of 5HT-induced modulation of spike broadening and increased excitability. The resulting dose-response curve showed that both forms of modulation increase monotonically as a function of 5HT concentration, but that excitability has a lower threshold for modulation by 5HT than does spike duration. 3. We further characterized the modulatory effects of 5HT on Aplysia SNs by comparing the time course of onset of modulation by 5HT and the time course of recovery after washout. Independent of 5HT concentration, modulation of excitability increases rapidly in the presence of 5HT and recovers rapidly (< 3 min) after washout. Similarly, input resistance increases and recovers rapidly, mirroring the profile of increased excitability. However, modulation of spike duration exhibits two profiles, dependent on 5HT concentration. Low concentrations of 5HT (0.5 and 1 microM) induce a rapid-onset and transient-recovery form of spike broadening, which resembles the kinetics of increased excitability and increased input resistance. Higher concentrations of 5HT (2.5 and 5 microM) induce a more slowly developing and prolonged-recovery form of spike broadening (> 9 min). At these higher concentrations, the recovery profile for prolonged spike broadening is significantly different from those observed for both increased excitability and increased input resistance. 4. We next compared the relationship between spike broadening and short-term synaptic facilitation. We found that significant facilitation of synaptic transmission requires a high 5HT concentration, which is comparable with that required to induce prolonged spike broadening. Similarly, the recovery profiles for spike broadening and synaptic facilitation are strikingly similar, recovering in parallel. 5. Our experiments show that the modulatory effects of 5HT in the tail SNs can be dissociated both by their sensitivity to different concentrations of 5HT and by their kinetics of serotonergic modulation. Based on these results, together with extensive evidence from other laboratories, we propose that the short-term modulatory effects of 5HT fall into two distinct functional classes. The first class, which includes excitability, input resistance, and transient spike broadening, has a low threshold for 5HT modulation and recovers rapidly. The second class, which includes prolonged spike broadening and short-term synaptic facilitation, has a higher threshold for modulation and recovers more slowly. It now will be of interest to determine the functional contribution of each of these classes to different aspects of sensitization.

scholarly journals Calculating Event-Triggered Average Synaptic Conductances From the Membrane Potential

2007 ◽  
Vol 97 (3) ◽  
pp. 2544-2552 ◽  
Author(s):  
Martin Pospischil ◽  
Zuzanna Piwkowska ◽  
Michelle Rudolph ◽  
Thierry Bal ◽  
Alain Destexhe
Keyword(s):  
Membrane Potential ◽  
Cortical Neurons ◽  
Time Course ◽  
Spike Generation ◽  
Nonlinear Contribution ◽  
Central Neurons ◽  
Time Courses ◽  
Model Subject ◽  
Synaptic Conductances

The optimal patterns of synaptic conductances for spike generation in central neurons is a subject of considerable interest. Ideally such conductance time courses should be extracted from membrane potential ( Vm) activity, but this is difficult because the nonlinear contribution of conductances to the Vm renders their estimation from the membrane equation extremely sensitive. We outline here a solution to this problem based on a discretization of the time axis. This procedure can extract the time course of excitatory and inhibitory conductances solely from the analysis of Vm activity. We test this method by calculating spike-triggered averages of synaptic conductances using numerical simulations of the integrate-and-fire model subject to colored conductance noise. The procedure was also tested successfully in biological cortical neurons using conductance noise injected with dynamic clamp. This method should allow the extraction of synaptic conductances from Vm recordings in vivo.

scholarly journals Recovery of Growth Hormone Release from Suppression by Exogenous Insulin-Like Growth Factor I (IGF-I): Evidence for a Suppressive Action of Free Rather Than Bound IGF-I1

1998 ◽  
Vol 83 (8) ◽  
pp. 2836-2842
Author(s):  
Ian M. Chapman ◽  
Mark L. Hartman ◽  
Karen S. Pieper ◽  
Emily H. Skiles ◽  
Suzan S. Pezzoli ◽  
...  
Keyword(s):  
Growth Factor ◽  
Time Course ◽  
Temporal Association ◽  
Saline Control ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Rebound Increase ◽  
Serum Gh

abstract To determine the time course of recovery of GH release from insulin-like growth factor I (IGF-I) suppression, 11 healthy adults (18–29 yr) received, in randomized order, 4-h iv infusions of recombinant human IGF-I (rhIGF-I; 3 μg/kg·h) or saline (control) from 25.5–29.5 h of a 47.5-h fast. Serum GH was maximally suppressed within 2 h and remained suppressed for 2 h after the rhIGF-I infusion; during this 4-h period, GH concentrations were approximately 25% of control day levels [median (interquartile range), 1.2 (0.4–4.0) vs. 4.8 (2.8–7.9) μg/L; P &lt; 0.05]. A rebound increase in GH concentrations occurred 5–7 h after the end of rhIGF-I infusion [7.6 (4.6–11.7) vs. 4.3 (2.5–6.0) μg/L; P &lt; 0.05]. Thereafter, serum GH concentrations were similar on both days. Total IGF-I concentrations peaked at the end of the rhIGF-I infusion (432 ± 43 vs. 263 ± 44 μg/L; P &lt; 0.0001) and remained elevated 18 h after the rhIGF-I infusion (360 ± 36 vs. 202 ± 23 μg/L; P = 0.001). Free IGF-I concentrations were approximately 140% above control day values at the end of the infusion (2.1 ± 0.4 vs. 0.88 ± 0.3 μg/L; P = 0.001), but declined to baseline within 2 h after the infusion. The close temporal association between the resolution of GH suppression and the fall of free IGF-I concentrations, and the lack of any association with total IGF-I concentrations suggest that unbound (free), not protein-bound, IGF-I is the major IGF-I component responsible for this suppression. The rebound increase in GH concentrations after the end of rhIGF-I infusion is consistent with cessation of an inhibitory effect of free IGF-I on GH release.

Sign in / Sign up

Export Citation Format

Share Document